Venous hypercarbia associated with severe sepsis and systemic hypoperfusion

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Abstract
We studied 37 patients with severe sepsis and systemic hypoperfusion to assess changes in PCO2. Before fluid administration, the cardiac index (CI) was 2.64 ± 0.14 L/min. m2. The PCO2 was 38 ± 1 torr and mixed venous pH was 7.32 ± 0.02. The venous-arterial CO2 tension gradient (P[-a]CO2) was 6 ± 1 torr. After fluid administration, the CI increased to 3.45 ± 0.14 L/min. m2 (p <.001) and the P(-a)CO2 decreased to 5 ± 1 torr. The correlation between the change in CI and the change in P(-a)CO2 was r =.42, p <.01. P(-a)CO2 was elevated in 19 (51%) patients before fluid administration (P[-a]CO2 >6 torr) (hypercarbic group). The P(-a)CO2 gradient in this group was 9 ± 1 compared with 4 ± 1 torr in 18 patients with a normal P(-a)CO2 gradient (p <.001) (normocarbic group). PCO2 was 41 ± 2 torr in the hypercarbic group compared with 35 ± 2 torr in the normocarbic group (p <.05). No difference was noted in PaCO2. Venous arterial pH and HC−O gradients were of greater magnitude in the hypercarbic group, −0.05 ± 0.003 and 2.4 ± 0.3 mEq/L compared to −0.02 ± 0.004 (p <.001) and 1.1 ± 0.2 mEq/L (p <.001), respectively. CI in the hypercarbic group was 2.3 ± 0.2 compared to 3.0 ± 0.2 L/ min. m2 in the normocarbic group (p <.05). Fluid administration resulted in a decrease in P(-a)CO2 from 9 ± 1 to 5.9 ± 0.8 torr in the hypercarbic group (p <.01). This was associated with a significant increase in CI from 2.3 ± 0.2 to 3.4 ± 0.2 L/min. m2 (p <.001). The correlation between the change in CI and the change in P(-a)CO2 was r =.46, p <.01. These data suggest that venous hypercarbia contributes to the acid-base disturbances associated with sepsis and circulatory failure. Furthermore, the development of venous hypercarbia is related to decreases in systemic blood flow.